S100A11 promotes TGF-β1-induced epithelial–mesenchymal transition through SMAD2/3 signaling pathway in intrahepatic cholangiocarcinoma

Abstract

Aim: Our previous study found S100A11 was significantly raised in intrahepatic cholangiocarcinoma cells, but the relationship between S100A11 and intrahepatic cholangiocarcinoma remains unclear. Methods: We investigated the effect of silencing S100A11 on TGF-β1-induced epithelial–mesenchymal transition (EMT), cell migration and invasion. Results: Our results demonstrated silencing S100A11 inhibited TGF-β1-induced cell migration, invasion and EMT, expression of EMT markers E-cadherin, N-cadherin, β-catenin, vimentin, Slug and Snail was reversed. Furthermore, TGF-β1-induced p-SMAD2 and 3 were also inhibited due to low S100A11 expression. Conclusion: Our present study indicated that S100A11 promotes EMT through accumulation of TGF-β1 expression, and TGF-β1-induced upregulation of p-SMAD2 and 3.